Bioassay of endothelium-derived relaxing factor(s): inactivation by catecholamines.

Bioassay of endothelium-derived relaxing factor(s): inactivation by catecholamines.
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内皮源性舒张因子的生物测定:儿茶酚胺灭活。

DOI:
10.1152/ajpheart.1985.249.1.h95
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发表时间:
1985
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
P. Vanhoutte
P. Vanhoutte
中科院分区:
--
文献类型:
--
作者:
G. Rubanyi;R. Lorenz;P. Vanhoutte

文献摘要

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建立了一种生物测定技术,用于分析内皮细胞释放的血管活性物质的作用。在37 ℃下用生理盐水灌注有或无内皮的犬股动脉。用无内皮的冠状动脉环对灌流液进行生物测定。内皮细胞在基础条件下释放的一种物质,引起未受刺激的冠状动脉舒张或前列腺素F2 α收缩的冠状动脉舒张。乙酰胆碱可增强松弛物质的释放。乙酰胆碱引起的舒张是双相的:一个初始的快速阶段,随后是部分恢复和缓慢发展的延长舒张;引起初始阶段的物质的半衰期平均为6.3 s。去甲肾上腺素,肾上腺素,抗坏血酸,给予股动脉下游,可逆地阻止了第二阶段,但只衰减了初始松弛。这些观察结果表明,在基础条件下和乙酰胆碱刺激期间,内皮源性舒张物质释放到股动脉腔内。儿茶酚胺可以抑制舒张物质,但不能阻止内皮细胞产生舒张物质或抑制舒张物质对血管平滑肌的作用。
A bioassay technique was developed to analyze the effect of vasoactive substance(s) released from endothelial cells. Canine femoral arteries with or without endothelium were perfused with physiological salt solution at 37 degrees C. The perfusate was bioassayed with a ring of coronary artery without endothelium. A substance(s) released by the endothelial cells under basal conditions caused relaxation of unstimulated coronary arteries or relaxation of those contracted with prostaglandin F2 alpha. The release of the relaxing substance(s) was augmented by acetylcholine. The relaxation induced by acetylcholine was biphasic: an initial rapid phase followed by a partial recovery and a slowly developing prolonged relaxation; the half-life of the substance(s) causing the initial phase averaged 6.3 s. Norepinephrine, epinephrine, and ascorbic acid, given downstream of the femoral artery, reversibly prevented the second phase but only attenuated the initial relaxation. These observations indicate that an endothelium-derived relaxing substance(s) is released into the lumen of the femoral artery under basal conditions and during stimulation with acetylcholine. Catecholamines can inactivate the relaxing substance(s) but do not prevent either its production by endothelial cells or its action on vascular smooth muscle.